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Adhesion G protein-coupled receptor Gpr126/Adgrg6 is essential for placental development

Rebeca Torregrosa-Carrión1,2, Rebeca Piñeiro-Sabarís1,2, Marcos Siguero-Álvarez1,2

  • 1Intercellular Signalling in Cardiovascular Development and Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Melchor Fernández Almagro 3, 28029 Madrid, Spain.

Science Advances
|November 12, 2021
PubMed

Insights

Mutations in GPR126/ADGRG6 impact peripheral nervous system myelination. Placental GPR126 is crucial for embryonic survival and preventing heart defects, suggesting a placenta-heart axis role in GPR126-related diseases.

Area of Science:

  • Developmental Biology
  • Genetics
  • Cell Biology

Background:

  • Mutations in G protein-coupled receptor GPR126/ADGRG6 are linked to human diseases, notably defective peripheral nervous system (PNS) myelination.
  • Understanding GPR126 function is critical for addressing these genetic disorders.

Purpose of the Study:

  • To investigate the role of GPR126 in embryonic development and disease pathogenesis.
  • To generate and characterize novel genetic models for GPR126 research.

Main Methods:

  • Generation of genetic mouse and zebrafish models with Gpr126 mutations.
  • Analysis of Gpr126 expression patterns in embryonic tissues, including the heart and placenta.
  • Assessment of embryonic lethality, heart development, PNS myelination, and placental function in mutant models.

Main Results:

  • Global Gpr126 inactivation in mice leads to embryonic lethality with cardiac abnormalities, but endocardial-specific deletion does not affect heart development.
  • Zebrafish gpr126 mutants show normal heart development.
  • Placental GPR126 expression is essential for embryonic survival; Gpr126 deficiency in the placenta down-regulates preeclampsia markers and causes PNS defects in surviving mice.

Conclusions:

  • GPR126 plays a vital role in placental development, which is essential for embryonic survival and preventing secondary heart abnormalities.
  • A placenta-heart axis is proposed to mediate heart defects observed in GPR126-deficient embryos, highlighting the placenta's systemic influence.

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